The physiological mechanisms of atrial tachyarrhythmias are often single, stable, reentrant circuit of very short cycle duration, which drives the atria, producing arrhythmic conduction. A reentrant circuit is typically a physical and electrical feedback loop composed of cardiac cells that repeatedly cycle electrical impulses in a tight circle and spin off abnormal impulses that propagate over the heart atrial tachycardia. Such a problem feedback loop or “driver,” may be originated by a “trigger,” such as an abnormally occurring spontaneous depolarization of cell membrane in the myocardial tissue. Drivers are typically very regular, and each trigger can initiate many variations of these reentrant pathways. Resulting reentrant circuits can be large or small, i.e., a macro reentrant circuit, or instead, a small micro reentrant circuit, e.g., less then 1 mm in diameter. These small drivers can even mimic a trigger, although they are really small reentrant circuits.
A typical cycle duration for such a reentrant circuit is on the order of 100-200 milliseconds (ms). This is the equivalent of 600 beats per minute at a 100 ms cycle duration. If there is no such trigger and no resulting reentrant circuit, then tachyarrhythmia conduction will not be there, i.e., the electrical conduction will be normal intrinsic conduction from an intrinsic rhythm (e.g., normal sinus rhythm).
Reentrant circuits can be further understood in terms of cellular action potentials continually propagating around the reentrant circuit at a rate considerably faster than the heart's intrinsic rate, provided that the reentrant wave front, i.e. the head of the propagation wave front, moves slowly enough that tissue ahead recovers excitability, i.e., slowly enough that a tail or end of the propagation wave front can form. The spatial extent of unexcitable tissue in this circuit is termed the reentrant wavelength, and is approximated by the product of the head's velocity and the action potential duration. As long as the wavelength is less than the circuit's perimeter, i.e. the reentrant path length, the head and tail remain separated by an “excitable gap” of tissue waiting to be stimulated. Termination of anatomic reentry requires elimination of the excitable gap, which can be achieved by appropriate pacing. An appropriately timed pacing pulse will initiate action potentials that propagate in both directions, colliding with the head and “blocking in” the tail.
In more simplified terms, the reentrant circuit can be thought of as a conduction wave front propagating along a tissue mass of somewhat circular geometry. This circular conduction will consist of a portion of refractory tissue and a portion of excitable tissue. To terminate the circuit, a pacing stimulus should be provided at the time and location when the tissue just comes out of refractoriness. If this occurs, the paced stimulation wave front proceeds toward the advancing wave front of the circuit, colliding with the wave front and interrupting the circuit. If the pacing stimulus arrives too soon it will be ineffective because the tissue will still be in refractoriness. If the stimulus arrives too late, it will generate wave fronts both towards the advancing wave front and towards the tail of the circuit. Although one pacing-generated wave front will collide with the advancing wave front of the reentrant circuit and will halt is progress, the latter pacing-generated wave front will act to sustain the reentrant circuit.
Anti-tachycardia pacing (ATP) is a standard treatment option to terminate most reentrant tachycardias. Overdrive pacing techniques to interrupt or to prevent tachycardias virtually always are performed by pacing from a single-site. Studies, however, have demonstrated that rapid pacing from a single-site can be proarrhythmic due to production of conduction abnormalities which may contribute to the onset and maintenance of atrial tachyarrhythmias.
Recent studies in normal and abnormal atria have demonstrated that linear triple site rapid bipolar pacing, compared with single site bipolar rapid pacing, produces 1) more uniform linear activation wave fronts; 2) shorter right atrial and bi-atrial activation time and faster mean epicardial speed; and 3) velocity vectors with a more uniform magnitude and direction. It has been suggested that a concave (i.e., curving inward) wave front creates more rapid depolarization in front of the advancing wave front compared with a flat wave front pattern. This is because the local excitatory current of the concave wave front pattern is larger than that of the flat wave front pattern. When the wave front is convex (i.e., curving outward), the wave front travels more slowly than the flat wave front, because the local excitatory current is distributed over a larger area in front of the wave front than the flat wave front. See Comparative Effects of Single- and Linear Triple-site Rapid Bipolar Pacing on Atrial Activation in Canine Models, Ryu et al., Am J Physiol Heart Circ Physiol, Vol. 289.